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Medicine I > Respiratory - Noninfectious Pulmonary Parenchymal Disease > Flashcards

Respiratory - Noninfectious Pulmonary Parenchymal Disease Flashcards

1
Q

What happens when Carbon monoxide (CO) is inhaled?

A
  • Forms Carboxyhemoglobin
    • CO has 200x greater affinity for hemoglobin
    • Less O2 carried in blood
    • Less O2 released at tissues (holds on tight)
  • Mucus membranes can be red but oxygen is not as available to tissues
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2
Q

What is Cyanide Toxicosis?

A
  • Produced by combustible items as they burn
  • Cyanide inhibits cytochrome oxidase
    • inhibits aerobic metabolism
  • CNS and heart depend on aerobic ATP production
  • Almond odor
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3
Q

What are the respiratory concerns with fire patients?

A
  • Tissue Hypoxia:
    • ⇣ inspired, carrying, and release of O2
    • Cardio (arrhythmias), Neuro (sedate, seizures, coma)
  • Thermal Damage
    • Upper respiratory tract and larynx
    • Dermal burns
  • Pulmonary Irritation
    • Toxins cause chemical or thermal-induced bronchoconstriction, inflammation, necrosis, pulmonary edema
    • Signs range from ⇡RR to fatal respiratory dysfunction
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4
Q

What can be seen on radiographs of fire patients?

A
  • Can be normal in mild cases (20%)
  • Can show bronchial disease from toxin irriation
  • Can show pulmonary edema
    • inflammation and oxidant injury damage alveoli and increase permeability
    • blood flow increased and lymphatics impaired
  • Can show alveolar pattern
    • pneumonia can occur after smoke inhalation
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5
Q

What are the treatments for Fire patients?

A
  • Respiratory Tract:
    • O2 supplementation to eliminate CO
      • hyperbaric oxygen chamber can help
    • Bronchodilators
    • Nebulization and coupage
    • Other potential therapies
      • Antibiotics if documented pneumonia
      • Steroids if obstructive airway edema/inflammation
      • Tracheostomy f obstruction
      • +/- mechanical ventilation
    • Burns: wound care, antibiotics, IV fluids, analgesia
    • Eyes: Topical antibiotics and atropine
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6
Q

What does a Hyperbaric Oxygen Chamber do?

A
  • Patient breathes 100% Oxygen intermittently inside a chamber with increased pressure
    • More O2 dissolved in blood
    • ⇡ availability to tissues (12-15x)
    • Allows CO elimination too
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7
Q

What is Pulmonary edema? causes?

A
  • Pulmonary Edema = increased fluid in the extravascular pulmonary parenchyma
    • Cardiogenic (congestive heart failure)
      • increased hydrostatic pressure due to falling heart and fluid overload
      • Non-cardiogenic
        • increased permeability of vessels from damage to microvascular barrier, causes leaking fluid and protein into interstitium and alveoli
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8
Q

What is the clinical presentation of Pulmonary edema?

A
  • Dyspnea, cough
    • may cough up pinkish foam
  • Harsh and moist sounding lungs (crackles)
  • listen closely for murmur
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9
Q

How should a patient with pulmonary edema be radiographed?

A
  • DV less stressful than VD
  • Have oxygen available
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10
Q

What are the differentials for Noncardiogenic Pulmonary Edema?

A
  • Stepwise Diagnostics as needed O2 in between
    • Radiographs confirm edema and help with cardiac/noncardiogenic
    • Echo to confirm/ruleout cardiac disease if in question
    • Hx ad PE help prioritize/ruleout many noncardiogenic differentials
      • Oral ulcerations - think electrocution
      • Signs of infection/sepsis - CBC, Chem, cultures, titers
      • Non of the above? - is there systemic inflammation, neoplasia, neurologic disease
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11
Q

What is the treatment for noncardiogenic pulmonary edema?

A
  • Oxygen and low stress
  • Treat underlying disease
  • Furosemide:
    • helps if cardiac edema (congestive heart failure)
    • Ok to try 1 dose while sorting out reason for edema
    • willl not help noncardiogenic edema cases
      • may be harmful if patient is hypovolemic
  • Ventilator for severe cases
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12
Q

What is Acute Respiratory Distress Syndrome (ARDS)?

A
  • Exaggerated inflammatory response in the lungs
    • sequelae to acute lung injury, systemic inflammation or sepsis
    • Cytokines infiltrate, chemotaxis of neutrophils and macrophages
    • Permeability of pulmonary vessels keeps increasing
      • Non-cardiogenic edema worsens
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13
Q

What is Pulmonary Thromboembolism?

A
  • Obstruction of a pulmonary vessel with a blood clot originating at some distant site
  • Risk factors:
    • Virchow’s Triad-
      • vascular injury
      • Impaired blood flow (stasis)
      • hypercoagulability
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14
Q

What conditions result in hypercoagulable patients?

A
  • Protein losing nephropathy/enteropathy
  • Immune mediated hemolytic anemia
  • Neoplasia
  • Necrotizing pancreatitis
  • Cushing’s and steroid patients
  • Diabetes mellitus
  • Sepsis
  • Trauma
  • Cardiac Disease - not truly hypercoagulable, but ⇡ risk for emboli
    • heartworm, endocarditis, cardiomyopahty
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15
Q

What happens to pulmonary thromboembolisms?

A
  • Normal coagulation - clot starts lysing within several hours
  • Abnormal coagulation - existing clots can grow and more clots can form and travel
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16
Q

What are the clinical signs of Pulmonary Thromboembolism?

A
  • Vary from subclinical to acutely fatal
  • Acute onset dyspnea, tachypnea
    • Ventilation/perfusion mismatch
    • Hypoxia
  • Signs of underlying disease elsewhere
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17
Q

How is pulmonary Thromboembolism diagnosed?

A
  • Often suspected but hard to prove
  • Chest Radiographs
    • areas of hypovascular lung (VD/DV views)
    • Pulmonary infiltrates (hemorrhage, atelectasis, infarct)
  • Coagulation Testing
    • PT/PTT/platelets - no correlation between these and thromboembolism
    • Low antithrombin III concentration increases thrombotic risk
    • Higher D-Dimer concentration is consistent with PRE
      • D-dimer = plasmin-mediated break
  • Try to confirm with:
    • pulmonary angiography
    • Nuclear scintigraphy
18
Q

What is the treatment for Pulmonary thromboembolism?

A
  • Oxygen supplementation
  • IV fluids to optimize perfusion
  • Bronchodilator may help
    • Theophylline ⇢ pulmonary vasodilation
  • Prevent more Clots
    • Heparin 100 U/kg SQ TID
    • Aspirin 0.5-1.0mg/kg PO q24hrs
    • Clopidogrel 0.5-1mg/kg PO q24hrs
  • Treat underlying disease
19
Q

What are pulmonary contusions

A
  • Compression injury w/hemorrhage
    • injury to vessel walls causes non-cardiogenic edema and loss of lung compliance
  • Can be progressive in first 24-48hrs
    • may present with decent or good respiratory function
    • Can deteriorate quickly
    • if survive - resolve over 7-10days
  • most common thoracic injury in dogs/cats
    • Car accidents, falls, fights, abuse
20
Q

What are the clinical signs of pulmonary contusions

A
  • Can be mild at first
  • Then tachypnea, dyspnea, open-mouth breathing
  • Crackles, cyanosis, hemoptysis, ⇡HR, arrhythmias
21
Q

How are pulmonary contusions diagnosed?

A
  • Radiographs- patchy alveolar or interstitial pattern
    • may take 48hrs to appear
      • CT documents changes earlier
22
Q

What is the treatment for Pulmonary Contusions?

A
  • Treat life-threatening injuries
  • Oxygen supplementation
  • Pain control
  • Fluids to optimize perusion, but avoid fluid overload
    • may have increased vascular permeability ⇢ non-cardiogenic pulmonary edema
  • Monitor closely for 48hrs (may worsen quickly)
  • Ventilator for severe cases
23
Q

What is the pathophysiology of Lung lobe torsions

A
  • Lung torses and vein collapses but artery stays open
    • severe congestion causes fluid to leak into interstitium
    • lung consolidates, fluids leaks out, pleural effusion forms
  • Why?
    • Spontaneous, underlying respiratory disease, surgical trauma
      • Anything that causes consolidation or atelectasis in cobco with extra fluid or air surrounding the lobe could increase risk of torsion
24
Q

Which breeds have an increased risk of lung lobe torsions?

A
  • Large deep-chested dogs
    • Afgan hound 133x more likely than other breeds
  • Pugs increased risk
25
Q

What is the clinical presentation of patients with lung lobe torsion?

A
  • Dyspnea
  • coughing
  • depression
  • Dull lung sounds due to consolidation and effusion
26
Q

How is Lung lobe torsion diagnosed?

A
  • Thoracocentesis to improve breathing, fluid analysis
  • Radiographs - consolidation with air bronchogram
    • right middle or left cranial lobes (due to shape and looseness)
  • Ultrasound w/ Doppler: torsed hilus obstructed with fluid and lack of venous flow
  • Fluid Analysis (variable)
    • Clear
    • Serosanguinous/hemorrhagic
    • Chylous
    • Cytology:
      • neutrophils and lymphocytes
      • check for neoplasia and fungal disease
    • Culture usually negative
27
Q

What is the treatment for lung lobe torsion?

A
  • Remove fluid prior to surgery
    • Some dogs need chest tubes
    • Oxygen and IV fluids as indicated
  • Sx for lung lobectomy
28
Q

What is the prognosis for patients with lung lobe torsion

A
  • Most dogs do well if spontaneous or non-neoplastic
  • Afgans ⇡ risk for persistent chylothorax post-op
29
Q

What is the common signalment of Pulmonary Fibrosis patients?

A
  • Middle to older age dogs and cats
  • No sex predilection
  • Breeds:
    • West highland white terriers
    • Staffordshire bull terriers
    • Other terrier breeds
    • Miniature poodles
    • No specific cat breeds
30
Q

What is the Etiology of Pulmonary Fibrosis?

A
  • Primary Idiopathic
  • Genetic predisposition
  • Secondary
    • infectious
      • FIV, herpes, calicivirus, toxoplasmosis, histoplasmosis, COVID
    • Toxin- paraquat is a classic offender
    • Neoplasia
    • Systemic lupus erythematosus
31
Q

What is the pathophysiology of Pulmonary Fibrosis?

A
  • Damage to alveolar epithelium and Type I pneumocytes
  • Type II pneumocytes are more compact and less sensitive to injury - so they proliferate to fill in denuded areas
32
Q

What is the history and PE associated with Pulmonary Fibrosis?

A
  • Hx:
    • usually slowly progressive respiratory signs
      • BAR, good appetite
      • Exercise intolerance, tachypnea, dyspnea, cough
  • PE:
    • Abnormal auscultation
      • Crackles common, wheezes may be present
33
Q

How is Pulmonary Fibrosis diagnosed?

A
  • Radiographs
    • pronounced patchy diffuse pattern
    • Equal number of interstitial, alveolar, bronchial patterns; some mixed
  • Investigate other differentials or triggers that may be treatable (infectious) or not so treatable (neoplasia, paraquat)
  • Echo: may have pulmonary hypertension that we can treat
  • CT: classic honeycomb appearance in people
  • Lung aspirate:
    • not very helpful, unless able to assess architectural changes or degree of fibrosis
    • helps ID other diseases (cancer, fungal)
  • Lung biopsy:
    • Gold standard, but not always definitive
    • Patchy distribution means you can miss it
  • Dx is often presumptive based on breed and consistent signs and findings
34
Q

What is the treatment for Pulmonary Fibrosis?

A
  • Supplemental oxygen as needed
  • Immunosuppressive therapy (steroids, azathioprine - dogs only)
  • Anti-fibrotic therapy (steroids, +/- -colchicine)
  • Anti-pulmonary hypertension (sildenafil)
35
Q

What is Pulmonary Hypertension? Why does it occur?

A
  • Increase in pulmonary arterial pressure
  • sources:
    • ⇡ left atrial pressure
    • Pulmonary over-circulation
    • ⇡ pulmonary vascular resistance
36
Q

What leads to pulmonary hypertension?

A
  • Severe respiratory disease
    • Decreased oxygen exchange ⇢ Hypoxia
    • Hypoxia ⇢ vascular constriction and hypertrophy of pulmonary arterial walls
  • Underlying respiratory causes
    • Fibrosis, pneumonia, chronic bronchitis
    • Also seen with PTE, HW, shunts, mitral disease
37
Q

What are the clinical signs of pulmonary hypertension

A
  • Cough
  • Dyspnea
  • Cyanosis
  • Collapse
38
Q

What are the diagnostic tests for pulmonary hypertension

A
  • Thoracic radiographs - assess lungs for primary respiratory disease
  • Echocardiogram is most practical way
    • measure increased pulmonary artery pressure
39
Q

What is the treatment for Pulmonary Hypertension?

A
  • Sildenafil to relax pulmonary vasculature
40
Q

What primary lung tumors are found in dogs? signs? treatment?

A
  • Single mass, often incidental finding
  • Usually carcinomas, spread locally
  • Clinically normal or cough, dyspnea, hemoptysis
  • Often can be surgically removed
41
Q

What primary lung tumors are found in cats? signs? treatment?

A
  • Bronchogenic carcinomas, metastasize to digits
  • Radiographs extremely variable
  • Present with progressive dyspnea, increased effort

Medicine I (43 decks)

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